Evidence map›Paper›PMID 37196932›Full record

ArticleJournal of affective disorders2023

Glycoprotein acetyls and depression: Testing for directionality and potential causality using longitudinal data and Mendelian randomization analyses.

Daisy C P Crick, Eleanor Sanderson, Hannah Jones, Neil Goulding, Maria Carolina Borges, Gemma Clayton, Alice R Carter, Sarah Halligan, Deborah A Lawlor, Golam M Khandaker and 1 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of affective disorders, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.3field-weighted citation impact, top 22% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

7 citing papers in PubMed, 13 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 4 institutions in 2 countries.

Daisy C P CrickPopulation Health Sciences, Bristol Medical School, University of Bristol, Bristol, UK; MRC Integrative Epidemiology Unit at the University of Bristol, Bristol, UK. Electronic address: dc15053@bristol.ac.uk.
Eleanor SandersonPopulation Health Sciences, Bristol Medical School, University of Bristol, Bristol, UK; MRC Integrative Epidemiology Unit at the University of Bristol, Bristol, UK.
Hannah JonesPopulation Health Sciences, Bristol Medical School, University of Bristol, Bristol, UK; MRC Integrative Epidemiology Unit at the University of Bristol, Bristol, UK.
Neil GouldingPopulation Health Sciences, Bristol Medical School, University of Bristol, Bristol, UK; MRC Integrative Epidemiology Unit at the University of Bristol, Bristol, UK.
Maria Carolina BorgesPopulation Health Sciences, Bristol Medical School, University of Bristol, Bristol, UK; MRC Integrative Epidemiology Unit at the University of Bristol, Bristol, UK.
Gemma ClaytonPopulation Health Sciences, Bristol Medical School, University of Bristol, Bristol, UK; MRC Integrative Epidemiology Unit at the University of Bristol, Bristol, UK.
Alice R CarterPopulation Health Sciences, Bristol Medical School, University of Bristol, Bristol, UK; MRC Integrative Epidemiology Unit at the University of Bristol, Bristol, UK.
Sarah HalliganDepartment of Psychology, University of Bath, Bath, UK; Department of Psychiatry and Mental Health, University of Cape Town, South Africa.
Deborah A LawlorPopulation Health Sciences, Bristol Medical School, University of Bristol, Bristol, UK; MRC Integrative Epidemiology Unit at the University of Bristol, Bristol, UK.
Golam M KhandakerPopulation Health Sciences, Bristol Medical School, University of Bristol, Bristol, UK; MRC Integrative Epidemiology Unit at the University of Bristol, Bristol, UK; NIHR Bristol Biomedical Research Centre, Bristol, UK; Avon and Wiltshire Mental Health Partnership NHS Trust, Bristol, UK.
Abigail FraserPopulation Health Sciences, Bristol Medical School, University of Bristol, Bristol, UK; MRC Integrative Epidemiology Unit at the University of Bristol, Bristol, UK.
MRC Epidemiology Unit · GBUniversity of Bristol · GBNIHR Bristol Biomedical Research Centre · GBUniversity of Cape Town · ZA

Funding

British Heart Foundation AA/18/7/34219Medical Research Council G9815508Medical Research Council MC_PC_15018Medical Research Council MC_PC_17213Medical Research Council MC_PC_19009Medical Research Council MC_UU_00011/6Medical Research Council MC_UU_00032/6Medical Research Council MR/L022206/1Medical Research Council MR/N0137941/Medical Research Council MR/P014054/1Medical Research Council MR/S037675/1Medical Research Council MR/W014416/1Wellcome Trust 201486Wellcome Trust 201486/Z/16/ZWellcome Trust 217065Wellcome Trust 217065/Z/19/ZWellcome Trust 76467/Z/05/ZWellcome Trust 8426812/Z/07/Z
6 · The paper itself

Abstract

backgroundInflammation is associated with depression, but causality remains unclear. We investigated potential causality and direction of effect between inflammation and depression.

methodsUsing data from the ALSPAC birth cohort (n = 4021; 42.18 % male), we used multivariable regression to investigate bidirectional longitudinal associations of GlycA and depression and depression symptoms, assessed at ages 18y and 24y. We used two-sample Mendelian randomization (MR) to investigate potential causality and directionality. Genetic variants for GlycA were obtained from UK Biobank (UKB) (N = 115,078); for depression from the Psychiatric Genomics Consortium and UKB (N = 500,199); and for depressive symptoms (N = 161,460) from the Social Science Genetic Association Consortium. In addition to the Inverse Variance Weighted method, we used sensitivity analyses to strengthen causal inference. We conducted multivariable MR adjusting for body mass index (BMI) due to known genetic correlation between inflammation, depression and BMI.

resultsIn the cohort analysis, after adjusting for potential confounders we found no evidence of associations between GlycA and depression symptoms score or vice versa. We observed an association between GlycA and depression (OR = 1∙18, 95 % CI: 1∙03-1∙36). MR suggested no causal effect of GlycA on depression, but there was a causal effect of depression on GlycA (mean difference in GlycA = 0∙09; 95 % CI: 0∙03-0∙16), which was maintained in some, but not all, sensitivity analyses. LIMITATIONS: The GWAS sample overlap could incur bias.

conclusionWe found no consistent evidence for an effect of GlycA on depression. There was evidence that depression increases GlycA in the MR analysis, but this may be confounded/mediated by BMI.

Indexed as

DepressionMendelian Randomization AnalysisCausalityCohort StudiesFemaleGenome-Wide Association StudyHumansInflammationMalePolymorphism, Single NucleotideALSPACDepressionGlycoprotein acetylsInflammationMendelian randomization

Identifiers

PMID37196932
PMCPMC7615476
OpenAlexW4376891002

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.